selenoP Cancer Research Results

selenoP, selenoproteins: Click to Expand ⟱
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Selenoproteins are a group of proteins that incorporate the rare amino acid selenocysteine into their structure. Selenocysteine, sometimes called the “21st amino acid,” is encoded by the UGA codon in a unique context that requires specific translational machinery. Many selenoproteins are known for their antioxidant and redox-regulatory functions, which are critical in maintaining cellular homeostasis. These functions help protect cells from oxidative stress and damage—processes that, when dysregulated, can contribute to carcinogenesis.

Roles of Selenoproteins in Cancer.
1. Antioxidant Defense & Redox Regulation
-Glutathione Peroxidases (GPxs): Enzymes like GPX1, GPX2, and GPX3 reduce hydrogen peroxide and lipid hydroperoxides. This protects cells against oxidative DNA damage.
-Thioredoxin Reductases (TXNRDs): TXNRD1, TXNRD2, and TXNRD3 help maintain the reduced state of thioredoxin, thereby contributing to redox homeostasis and cell survival under stress.

2. Cellular Proliferation and Apoptosis -Selenoproteins may modulate signaling pathways that regulate cell cycle progression and apoptosis. Variations in expression levels—either upregulation or downregulation—can tip the balance toward uncontrolled cell growth or cell death.

The expression of selenoproteins in cancers is complex and can vary by tumor type. Here are some examples:

Glutathione Peroxidases (GPxs)
-GPX1: Both overexpression and underexpression have been reported depending on the tumor context. In some cases, high GPX1 expression can help cancer cells survive oxidative stress.
-GPX2: Often upregulated in colorectal cancer and some GC, poor prognosis.
-GPX3: Typically downregulated in many cancers with tumor progression and poor outcome, suggesting its role as a tumor suppressor.

Thioredoxin Reductases (TXNRDs)
-TXNRD1: Frequently overexpressed in various tumors such as lung, breast, and liver cancers.
High TXNRD1 levels are generally associated with a poor prognosis.
-SELENOP (Selenoprotein P) SELENOP serves as a selenium transport protein and has antioxidant properties. Decreased SELENOP expression has been linked to poorer outcomes in some cancers, possibly due to reduced selenium availability for other protective selenoproteins.

Other Selenoproteins
-SELENOF and SELENOS:
-SELENOM and SELENOK:
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
4492- Se,    Selenium in cancer prevention: a review of the evidence and mechanism of action
- Review, Var, NA
Risk↓, AntiCan↑, *selenoP↑, TumMeta↓, *DNAdam↓, OS↑, *ROS↓,
4724- Se,    Chapter Four - Selenium in the Redox Regulation of the Nrf2 and the Wnt Pathway
- Review, Var, NA
Risk↓, *selenoP↑, other↝, Risk↓,
4717- Se,    A systematic review of Selenium as a complementary treatment in cancer patients
- Review, Var, NA
*antiOx↑, eff↝, radioP↑, chemoP↑, *selenoP↑, *GPx↑, TrxR↑, *ROS↓,
4712- Se,    Selenium and selenoproteins: key regulators of ferroptosis and therapeutic targets in cancer
- Review, Var, NA
selenoP↑, Ferroptosis↑, lipid-P↑,
4719- SeNPs,    Selenium nanoparticles are more efficient than sodium selenite in producing reactive oxygen species and hyper-accumulation of selenium nanoparticles in cancer cells generates potent therapeutic effects
- in-vivo, Var, NA
ROS↑, selenoP↑, *toxicity↓,
4609- SeNPs,    Physiological Benefits of Novel Selenium Delivery via Nanoparticles
- Review, Var, NA - Review, IBD, NA - Review, Diabetic, NA
*selenoP↑, Risk↓, AntiCan↑, ROS↑, *Dose↝, *toxicity↓, *BioAv↑, *GutMicro↑, *other↓,
4608- SeNPs,    Selenium Nanoparticles for Biomedical Applications: From Development and Characterization to Therapeutics
- Review, Var, NA - NA, AD, NA
*toxicity↝, *toxicity↓, *other↝, ROS↑, *Dose↝, *selenoP↑, AntiCan↑, AntiTum↑, *Bacteria↓, *radioP↑, *BioAv↑, *Inflam↓, *Imm↑, ChemoSen↑, *AntiAg↑, selectivity↑, eff↑, other↝, *eff↑, *Aβ↓, *eff↑,
4457- SeNPs,    Selenium nanoparticles: a review on synthesis and biomedical applications
- Review, Var, NA - NA, Diabetic, NA
*BioAv↑, *toxicity↓, *eff↑, chemoPv↑, *Inflam↓, antiOx↑, *selenoP↑, *ROS↓, *Dose↝, AntiCan↑, *Bacteria↓, eff↑, DNAdam↑, selectivity↑, *eff↑,
4739- SSE,  Chemo,  Rad,    Therapeutic Benefits of Selenium in Hematological Malignancies
- Review, Var, NA
ChemoSen↑, radioP↑, QoL↑, Risk↓, *selenoP↑, TumCP↓, Inflam↓, ChemoSen↑, TumCCA↑, Apoptosis↑, angioG↓, Dose⇅, ROS↑, eff↑, Risk↓, eff∅, CSCs↓, ROS↑,
4740- SSE,    Optimising Selenium for Modulation of Cancer Treatments
- Review, Var, NA
*selenoP↑, *Dose↓, Risk↓, *toxicity↝, Dose↑, chemoP↑, radioP↑,
4610- SSE,  Rad,    Protection during radiotherapy: selenium
- Review, Var, NA
*radioP↑, *antiOx↑, *Inflam↓, *DNAdam↓, *lipid-P↓, *selenoP↑, *GPx1↑, *BUN↓,
4498- SSE,    Selenium in Human Health and Gut Microflora: Bioavailability of Selenocompounds and Relationship With Diseases
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
*Imm↑, *GutMicro↑, *BioAv↑, *Risk↓, *Dose↝, Risk↓, *CRP↓, *GPx↓, *Inflam↓, *selenoP↑, *Dose↝, *ROS↓, *MDA↓, *SOD↑, *GPx↑, *IL1↓, *MCP1↓, *IL6↓, *TNF-α↓, Risk↓, *neuroP↑, *memory↑,
4497- SSE,    Selenium and inflammatory bowel disease
- Review, Var, NA - Review, IBD, NA
*GutMicro↑, *selenoP↑, *Inflam↓, Risk↓, *NF-kB↓, *ROS↓,
4494- SSE,    Advances in the study of selenium and human intestinal bacteria
- Review, IBD, NA - Review, Var, NA
*Risk↓, OS↑, *CRP↓, *GPx↑, *Inflam↓, *ROS↓, *GutMicro↑, *selenoP↑, *other↓,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Ferroptosis↑, 1,   lipid-P↑, 1,   ROS↑, 5,   selenoP↑, 2,   TrxR↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Ferroptosis↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,  

Migration ⓘ

TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   Dose↑, 1,   Dose⇅, 1,   eff↑, 3,   eff↝, 1,   eff∅, 1,   selectivity↑, 2,  

Functional Outcomes ⓘ

AntiCan↑, 4,   AntiTum↑, 1,   chemoP↑, 2,   chemoPv↑, 1,   OS↑, 2,   QoL↑, 1,   radioP↑, 3,   Risk↓, 10,  
Total Targets: 31

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   GPx↓, 1,   GPx↑, 3,   GPx1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   ROS↓, 6,   selenoP↑, 12,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

BUN↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,   other↝, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 2,  

Migration ⓘ

AntiAg↑, 1,  

Immune & Inflammatory Signaling ⓘ

CRP↓, 2,   IL1↓, 1,   IL6↓, 1,   Imm↑, 2,   Inflam↓, 6,   MCP1↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 4,   Dose↓, 1,   Dose↝, 5,   eff↑, 4,  

Clinical Biomarkers ⓘ

CRP↓, 2,   GutMicro↑, 4,   IL6↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   neuroP↑, 1,   radioP↑, 2,   Risk↓, 2,   toxicity↓, 4,   toxicity↝, 2,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 37

Scientific Paper Hit Count for: selenoP, selenoproteins
6 Selenite (Sodium)
4 Selenium
4 Selenium NanoParticles
2 Radiotherapy/Radiation
1 Chemotherapy
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:26  Cells:%  prod#:%  Target#:1172  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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